2024_Lecture 6 Respiratory Diseases.pdf

CASE REVIEW On a visit to a farm you observe numerous pigs exhibiting lesions as shown in the picture. 1) List three possible differential diagnoses stating the aetiological agent.  On further observation you notice the animals can be seen vigorou...

CASE REVIEW On a visit to a farm you observe numerous pigs exhibiting lesions as shown in the picture. 1) List three possible differential diagnoses stating the aetiological agent.  On further observation you notice the animals can be seen vigorously rubbing their flanks on the pen walls. State what samples you will collect to confirm your diagnosis 3) Recommend two possible treatment regimens for these animals indicating the therapeutic agent, route of administration and frequency. Respiratory Diseases Actinobacillus pleuropneumoniae a highly contagious disease of swine, characterized by severe pleuropneumonia with sudden onset, high morbidity, and high mortality.  Aetiology Actinobacillus pleuropneumoniae (APP) – Gram-negative – highly host-specific for swine. 16 serovars recognized – four (1, 3, 5, 7) are most common in North America. The organism does not persist for any significant time in the environment.  Aetiology Actinobacillus pleuropneumoniae (APP) The APP organism secretes 4 exotoxins called RTX toxins* – ApxI is strongly haemolytic and strongly cytotoxic produced by serovars 1,5a, 5b, 9, 10, 11, 14 and 16; – ApxII is weakly haemolytic and moderately cytotoxic, Produced by all serovars except for 10 and 14; – ApxIII is non‐haemolytic, strongly cytotoxic Produced by serovars 2, 3, 4, 6, 8 and 15. – ApxIV has not been characterised with regards to haemolytic or cytotoxic capacity Sassu EL, Bossé JT, Tobias TJ, Gottschalk M, Langford PR, Hennig‐Pauka I. Update on Actinobacillus pleuropneumoniae—knowledge, gaps and challenges. Transboundary and emerging diseases. 2018 May;65:72-90.  Epidemiology Widely distributed throughout major swine-raising countries. – Major problem in many European countries – Relatively common in the United States, Canada and Asia. Colostral immunity confers some resistance to infection – Permits gradual development of active immunity in many exposed, growing pigs. In naïve herds, APP occurs in all age groups – Most common in 6-20 week old pigs. – Clinical signs most severe in naïve herds.  Epidemiology Swine that survive acute APP often remain carriers. – Subclinical infected carriers with only occasional disease outbreaks Transmission: – Direct Contact – Aerosol transmission (short distances) – Fomites Risk Factors: – Co-infection with other respiratory pathogens – Overstocking – Inadequate ventilation – Any other stressor  Pathogenesis Hemolysin and other toxins act against endothelial cells and pulmonary alveolar macrophages Vasculitis within the lung Thrombosis Infarction Sudden death due to endotoxic shock  Clinical Signs Signs vary considerably between acute and chronic forms of APP. Acute: – Sudden death. – Early signs include: Recumbency High temperature Apathy, anorexia stiffness, +/- vomiting and diarrhea. Shallow, nonproductive cough is occasionally present. Marked dyspnea with mouth breathing and, perhaps, – a foamy, bloody discharge from the mouth and nose. Peripheral cyanosis of extremities. – As circulation fails, generalized cyanosis follows.  Clinical signs. Acute disease – Morbidity and mortality in growing swine varies but can become high. Peak mortality usually occurs in pigs 10-16 weeks old. Mortality can reach 20-80% in fattening pigs. Abortions may occur in acutely infected pregnant females. Chronic cases – may become apparent following an acute outbreak. – Chronic cough and slow growth rate Due to the presence of pleural adhesions and abscesses that form in recovered lungs  Lung Lesions Thoracic cavity often contains blood-tinged fluid Haemorrhage and necrosis in the dorsal portion of one or both diaphragmatic lobes Chronic cases – often have large areas of abscessation. – Lesion attached to the rib cage by fibrous adhesions LUNG LESIONS Actinobacillus pleuropneumoniae lung lesion Actinobacillus pleuropneumoniae lung lesion  Diagnosis Clinical signs – The sudden onset of an acute, rapidly-spreading, respiratory disease causing high morbidity and mortality is suggestive of APP. Must be differentiated from Actinobacillus suis Culture: Isolation and identification of APP is confirmatory. – Use of immunomagnetic separation may be required. Antibody test kits – Targeting the RTX toxin genes are also available facilitate differentiation from A. suis infection. Does not identify serotype present.  Treatment / Prevention/ Control Acute outbreaks – Antimicrobial therapy both parenteral and oral Affected animals and adjacent barns/pens – Commonly used agents Tiamulin, tulathromycin, chlortetracycline, ceftiofur, tilmicosin, florfenicol, enrofloxacin and procaine penicillin G. – Many strains are resistant to tetracyclines. Chronic cases – usually are unresponsive to treatment  Treatment / Prevention/ Control Control of APP in endemically infected herds requires combinations of vaccination, medication and improved husbandry. – Herds on premises free of APP should be managed as closed herds. – New stock obtained only from APP-free herds. – Testing and Quarantine period for at least 30 days prior to introduction. Management factors: – all in/all out production – Cleaning and disinfection between farrowings – Avoid overstocking – Proper ventilation – elimination or control of predisposing diseases.  Treatment / Prevention/ Control If APP is endemic in a sow farm: – Depopulation can be a cost-effective approach to eradication of the disease. Depopulation → thorough cleaning and disinfection→ pens vacant for a 3+ weeks → restocking with APP-free swine. – Alternatively, APP may be controlled in the offspring Segregated Early Weaning or Medicated early weaning Requirements: – First boosting immunity in the sows using serotype-specific antigens – assuring that piglets received adequate amounts of their colostrum, – weaning to a clean site – good biosecurity.  Prevention and Control: Vaccination Vaccination: – Autogenous bacterins are available Offers little cross protection between serotypes – Toxoid vaccine Stimulates immune response against toxins Greater protection against various serotypes. – Vaccination of piglets @ 5-7 weeks old Actinobacillus suis  Aetiology Actinobacillus suis – Gram-negative – non-motile coccobacillus. – All isolates appear to be of a single serotype. No serologic test to reliably identify infected swine and establish A. suis-free herds. Antibodies to A. suis and A. pleuropneumoniae may cross-react with some serologic tests  Epidemiology Not completely understood – Carrier pigs probably introduce A. suis into herds. Outbreaks occur predominantly in immunologically naïve populations. – Most outbreaks are in recently weaned pigs and in grow/finish pigs derived from an SEW system. – Outbreaks occur in both younger and older swine and, less often, in conventionally raised pigs A. suis has been isolated from – Nasal cavity and tonsils of many healthy pigs and reproductive tract of healthy sows.  Pathogenesis Invasion occurs through the tonsil or any cuts and spreads through the bloodstream. Pathogenic effect is similar to APP – Production of haemolysin and other toxins  Clinical signs. The first signs include sudden death of young pigs with lesions attributed to a bacterial septicaemia. – Sick piglets are febrile, breathe rapidly, +/- congested or cyanotic extremities. – Cyanosis, arthritis, enteritis rarely necrosis of the feet, tail and ears – Central nervous system (CNS) signs tremors, shaking or paddling. Mortality within affected litters can be up to 50%. Older growing pigs and adults rarely affected – +/-Signs of acute respiratory distress. Grower pigs – Lethargy, anorexia, depression  Diagnosis History and Clinical Signs are suggestive Confirmatory: Culture of A. suis from multiple organs (septicaemia). Serologic diagnosis is unreliable – Cross-reactions between antibodies to A. suis and APP  Treatment / Prevention/ Control Antimicrobials Vaccination – Sick pigs should be – Autogenous vaccines treated parenterally as have been used soon as possible. Multiple serotypes. – The exposed group can be treated by medicating the water. Amoxicillin Ceftiofur Penicillin Gentamicin (withdrawal period!) Mycoplasma hyopneumoniae Enzootic pneumonia.  Aetiology Mycoplasma hyopneumoniae, – A small, filterable, survives only a short time in swine housing environments and can be destroyed by most disinfectants. – Difficult to culture, slow growing in the laboratory. – Present in mixed infections May be a primary pathogen or secondary. Difficult to determine which agent is the primary pathogen.  Aetiology Other pathogenic strains of Mycoplasma – Mycoplasma hyosynoviae a sporadic cause of epidemic synovitis in growing swine. – Mycoplasma hyorhinis common cause of fibrinous polyserositis in young pigs  Epidemiology. Present in all major swine producing countries. Disease can be seen all year round. Acute and severe disease in immunologically naïve pigs in age-segregated systems. – Piglets affected early after weaning when passive immunity has waned – Higher incidence of disease in grower and finisher pigs Chronic disease seen on farms with: – continuous flow production and management – husbandry and environmental conditions are poor.  Epidemiology Carrier swine are the most common source of infection. – Short survival time in the environment – Carriers essential for disease propagation Persists for months in the lungs of infected pigs. Pigs are infected by M. hyopneumoniae transmitted from dams, cohorts, or exposure to other, usually older, pigs. The organism can be frequently isolated from nasal secretions Transmission: – nose-to-nose contact and coughing – Aerosol transmission Potentially several kilometres. A mycoplasma-free status of a herd can be difficult to maintain  Pathogenesis Colonises on ciliary epithelium of trachea, bronchi and bronchioles Bronchitis and bonchiolitis Hyperplasia of mucus secreting cells in the mucosa and loss of cilia Alveolitis, pneumonia, airway obstruction hyperplasia of lymphoid tissue, increased mucus in airways and ↓lung clearance of mucus and exudate. Secondary bacteria infection exacerbate pneumonia → deaths  Clinical Signs Chronic, persistent, nonproductive cough. – Onset 2-3 three weeks post exposure – Coughing may persist for weeks to months. Excessive dust, irritating gases, or concurrent infections result in more severe coughing. – As pneumonia progresses dyspnoea becomes more marked. – ↓Growth rate and ↓feed efficiency despite normal appetites. – Morbidity is high and mortality is low  Lung Lesions Pneumonic lesions well demarcated Lobes affected: – Cranioventral consolidation: involving apical, intermediate, and cardiac lobes May extend into diaphragmatic lobes in severe cases Cranioventral consolidation M. hyopneumoniae  Diagnosis History, signs, gross and microscopic lesions – suggestive but laboratory confirmation of M. hyopneumoniae required. Culture and Isolation – slow, laborious, difficult and generally not routinely available. Identification of the agent in lung samples taken at necropsy – fluorescent antibody – immunohistochemistry – polymerase chain reaction (PCR) techniques. Serologic tests available but vaccination status of animals has to be known. – Animals without active disease may have antibodies  Treatment/Control/Prevention Acute outbreaks: – Medicate pigs between weaning and 16 weeks of age for 4 to 8 weeks with 500g/tonne of CTC or OTC and then reduce this to 200- 300g/tonne. If pigs become affected soon after weaning inject with OTC LA at weaning time or one week prior to the onset of disease. – Inject severely affected individual pigs with either long-acting OTC, tiamulin, lincomycin, tilmicosin or penicillin/streptomycin. Chronic disease – Identify when disease onet most usually occurs Medication either in feed, in water or by injection using the medicines outlined above. E.g. For strategic medication use tetracyclines 500-800g/tonne for 7 to 10 prior to the anticipated time of the disease starting.  Treatment/Control/Prevention Vaccines effective in mitigating losses due to M. hyopneumoniae infection. – ↓lung lesions and ↑growth performance. – Two vaccination programs Sows are vaccinated once or twice several weeks before farrowing Vaccination of piglets before weaning and again two to three weeks later.  Treatment/Control/Prevention Strict biosecurity – Prevents entry Segregated Early Weaning OR Medicated Early Weaning Depopulation and Repopulation Antibiotics may augment management and vaccination techniques – Oral or via injection. – Lincomycin, tiamulin, tetracyclines, tylosin, tilmicosin, tulathromycin, enrofloxacin.  Atrophic Rhinitis Toxigenic strains of Bordetella bronchiseptica and Pasteurella multocida (primarily type D)  Aetiology Bordetella bronchiseptica – Gram-negative rod. – widely distributed in the swine population. – Readily colonizes the nasal passages of swine Septicaemia and suppurative bronchopneumonia in pigs up to 12 weeks old. – Isolated from many species other than swine (dogs, cats, rodents, rabbits, wildlife). Not believed to play a role in causing AR in swine. – Toxigenic porcine strains can cause atrophy of turbinates, particularly in pigs one to six weeks old. Lesions tend to be mild and can be largely repaired by the host and may not lead to progressive AR.  Aetiology Toxigenic Pasteurella multocida (type D) – less widespread in the swine population. – Often can be isolated from tonsils and lungs of swine +/- AR. +/- with B. bronchiseptica in outbreaks of AR. – Injury or insult to nasal mucous membrane ↑colonization of the nasal passages – Toxigenic P. multocida produces a potent dermonecrotizing toxin Causes marked turbinate atrophy as well as bony alterations in nasal and facial bones. – Turbinate lesions usually are initiated in pigs less than 16 weeks old but older pigs can be affected if immunologically naïve. – The lesions can persist for a lifetime  Epidemiology AR occurs in all swine producing countries. Propagation of AR on the farm: – Atrophic rhinitis results in the establishment of inapparent carriers. Swine introduced into a clean herd from an outside source can be carriers and disseminate the agents that cause AR. – Carrier sows expose their piglets. Infected piglets are mingled with others = ↑transmission. – Immune sows provide piglets with some colostral immunity Older sows may provide more colostral immunity than gilts But waning colostral immunity and weaning leave young pigs susceptible to infection.  Epidemiology Anything which causes insult to respiratory mucosa will increase predisposition to AR. Management or environmental factors: – Ventilation is an especially important factor. Irritating dust or ammonia from urine and faeces ↑severity of rhinitis → make nasal mucous membranes more susceptible to colonization by the primary agents of AR. – Other contributing factors include overstocking substandard housing sanitation continuous use of facilities failure to use all in/all out production methods.  Pathogenesis Environmental or microbial irritation of nasal passages Colonization with B. bronchiseptica and/or Pasteurella multocida B. bronchiseptica attached to P. multocida colonizes nasal ciliated epithelial cells mucosa secondary to B. bronchispetica and/or nasal mucosal insult Toxin diffuses into turbinates → osteopathy and hypoplastic rhinitis Toxigenic P. multocida produce a potent toxin → rhinitis with progressive osteopathy of facial Regeneration and repair can occur and turbinate bones ≡ progressive ≡ regressive atrophic rhinitis. atrophic rhinitis  Clinical Signs. one week old but most occur shortly after weaning. Sneezing, snorting and a serous or mucopurulent nasal discharge are early signs of AR. Rhinitis obstructs the flow of tears through the infraorbital ducts Signs caused by B. bronchiseptica alone tend to peak in a few weeks, and then diminish. Signs related to toxigenic P. multocida often appear in four to eight week old pigs and may persist for weeks or months.  Clinical Signs. Atrophic Rhinitis – Nosebleed in more acute outbreaks in weaned, growing pigs. – Growth retardation may become apparent. – Occasional pigs develop secondary bronchitis, bronchiolitis or pneumonia as an indirect effect of AR. A variable number of pigs develop lateral or dorsal deviation of the snout. Dorsal deviation often results in shortening of the snout or wrinkling of the skin over the snout. Marked snout deviation in many pigs usually is associated with toxigenic P. multocida  Clinical Signs Lesions are usually restricted to turbinates, nasal septum and nasal and facial bones – Observed by sawing transversely across the snout at the commissure of the lips 2nd premolar or 1st cheek tooth in pigs less than 6 months of age Lesions vary in severity and are usually graded on a scale of 0-5. – Minor lesions must be differentiated from normal variations in anatomy and breed character.  Nasal turbinates - normal Observed by sawing transversely across the snout at the commissure of the lips  Nasal turbinates - AR Observed by sawing transversely across the snout at the commissure of the lips  Diagnosis History, signs and lesions often are adequate for a clinical diagnosis of AR Confirmatory diagnosis: – Bacterial cultures made from nasal swabs from live or sacrificed pigs are most rewarding early in the course of infection (nursery). Differential diagnosis – Porcine reproductive and respiratory syndrome virus (PRRS), – pseudorabies virus (PRV), – inclusion body rhinitis (cytomegalovirus) – excessive dust or ammonia  Treatment / Prevention/ Control Improvement of husbandry, management and housing, including ventilation Vaccination program for the breeding stock, pigs, or both. – Bacterin-toxoid vaccines provide some protection and widely used. Adult animals vaccinated twice: 4 to 6 weeks apart. Sows often are vaccinated twice at about four and two weeks prior to parturition. Antimicrobial therapy. – Sows and piglets around the time of farrowing/weaning ↓ colonization in the young pigs. – Questionable efficacy in growing swine. Monitoring – Abattoir surveillance. Examination of the nasal passages of swine submitted for slaughter.  Treatment / Prevention/ Control Eradication of toxigenic P. multocida from a herd – Step 1: Combined medication and prefarrowing vaccination of sows. – Step 2: Litters and medicated and early weaned at 8-10 or 12-14 days. – Step 3: Nasal swabs of maturing animals tested via PCR for toxigenic P. multocida and infected animals are identified and eliminated Inclusion Body Rhinitis  Inclusion Body Rhinitis Aetiology: Porcine cytomegalovirus Subgroup of the herpesviruses. Ability to induce latent infection in carriers that can later be reactivated by stress. PCMV can be propagated in cell culture. – cell enlargement and formation of large intranuclear inclusion bodies.  Epidemiology PCMV occurs worldwide in the major swine- raising countries. Occurs in all age groups of previously uninfected swine, including developing foetuses. The presence of the virus within a herd often can be inapparent: – Sows immune +/- show no signs of infection – Colostral antibodies protect their young piglets from lesions as they are infected  Epidemiology Virus is shed during and for some time after infection. – Many infected piglets three to eight weeks old shed virus. – Virus is shed in nasal and ocular secretions, urine and the aerosol created by sneezing and coughing. Transmission of virus: – inhalation or ingestion of virus. – Recovered animals have virus sequestered as a latent infection and can then become shedders if stressed. Dissemination of virus when mixed with susceptible swine. Experimentally demonstrated to cross placenta to infect developing foetuses. – Infected foetuses may be killed, mummified, stillborn or born alive as infected, weak piglets. – Infected piglets then spread virus to susceptible piglets.  Pathogenesis The primary site of virus replication is believed to be in the nasal mucous glands or the lacrimal glands. – Destruction of their cells results in a marked rhinitis and conjunctivitis. Viremia follows replication. – The virus localizes in epithelial and endothelial cells The intracellular virus causes marked enlargement and destruction of many infected cells but persists and is tolerated by other cells. Endothelial cell damage and necrosis → petechial haemorrhages and oedema. Bone marrow damage causes anaemia in neonates. – Widespread damage caused by the virus or secondary infections can lead to death.  Clinical Signs The disease usually is observed in one to five week old pigs. – In suckling pigs < three weeks old: mucopurulent rhinitis accompanied by violent sneezing respiratory distress, conjunctivitis shivering, Mortality can be high in pigs born to naïve gilts or sows, or if PCMV is complicated by other diseases. – Infected neonatal piglets: appear weak, anaemic or stunted and there may be edema around the throat and tarsal joints.  Clinical Signs Signs in older pigs or dams with viremia may include listlessness and mild anorexia or may be inapparent. Naïve pregnant sows: Fetal mummification, stillbirths, neonatal deaths and failure of piglets to thrive  Diagnosis Microscopically: – Basophilic intranuclear inclusions in tissues of an infected piglet. Serology: – ELISA or indirect Immunofluorscent assay on serum samples..  Treatment / Prevention/ Control Control programmes not usually instituted – Disease not recognised or losses inapparent. Piglets initially protected by colostral antibodies until able to produce own. – Herd immunity via acclimatization of breeding stock. – No known effective antiviral or medication. Antibiotics may be useful to control concurrent diseases or secondary bacterial infections Necrotic Rhinitis  Necrotic Rhinitis Aetiology – Fusobacterium necrophorum Epidemiology – Low incidence – Entry during needle teeth clipping – Associated with young piglets – Poor sanitation increases incidence.  Necrotic Rhinitis Clinical Signs – loss of appetite → emaciation. – occasionally haemorrhage, snuffling, sneezing, foul-smelling nasal discharge – +/- involvement of the eyes with lacrimation and purulent discharge – Swelling and deformity of the face Incision of the facial swelling reveals a mass of pinkish to greenish-gray foul-smelling necrotic tissue. Deformity more severe if nasal and facial bones involved.  Necrotic Rhinitis Diagnosis – Evidence of abscessation Treatment/Prevention/Control – Prevention Good sanitation Avoid injuries to mouth and snout Proper needle clipping technique. – Treatment Not useful in late disease. Early surgical intervention and packing the cavity with sulfonamide or tincture of iodine may be useful. In young pigs, sulfamethazine given PO is of value (250mg/kg).  Review question Farmer Hamlet’s Pig farm tells you he recently bought some pigs and they have started dying suddenly. At around 12 weeks of age and some die suddenly. You observe many animals with a shallow, nonproductive cough while others have marked dyspnea and a foamy, bloody discharge from the mouth and nose. You also observe that some animals have peripheral cyanosis of extremities. (a) State three (3) infectious agents which may result in the clinical signs seen on this farm (for bacterial agents please list both genus and species).  Image 2: Image 1: Abscess within lung tissue dorsal portion of diaphragmatic lobe of lung (a) Image 1 exhibits lesions from the lung of one of the animals exhibiting dyspnoea while image 2 shows the lung tissue from one animal which recovered from the clinical signs but failed to thrive. State you tentative diagnosis: (b) DISCUSS YOUR TREATMENT PLAN THE END.